Herpes Simplex Virus

Herpes Simplex Virus

Q. 1 Infection with herpes simplex virus, a common human pathogen, is best described by which of the following statements?

A

The CNS and visceral organs are usually involved

B

It rarely recurs in a host who has a high antibody titer

C

It can be reactivated by emotional disturbances or prolonged exposure to sunlight

D

Initial infection usually occurs by intestinal absorption of the virus

Q. 1 Infection with herpes simplex virus, a common human pathogen, is best described by which of the following statements?

A

The CNS and visceral organs are usually involved

B

It rarely recurs in a host who has a high antibody titer

C

It can be reactivated by emotional disturbances or prolonged exposure to sunlight

D

Initial infection usually occurs by intestinal absorption of the virus

Ans.

C

Explanation:

The initial infection by herpes simplex virus is often inapparent and occurs through a break in the skin or mucous membranes, such as in the eye, throat, or genitals.Latent infection often persists at the initial site despite high antibody titers. Recurrent disease can be triggered by temperature change, emotional distress, and hormonal factors. Type 1 herpes simplex virus is usually, but not exclusively, associated with ocular and oral lesions; type 2 is usually, but not exclusively, associated with genital and anal lesions. Type 2 infection is more common. In addition to mucocutaneous infections, the CNS and occasionally visceral organs can be involved.

Q. 2

In herpes simplex encephalitis, drugs used are, EXCEPT:

A

Acyclovir

B

Vidarabine

C

Ganciclovir

D

Amantadine

Q. 2

In herpes simplex encephalitis, drugs used are, EXCEPT:

A

Acyclovir

B

Vidarabine

C

Ganciclovir

D

Amantadine

Ans.

D

Explanation:

The most effective drug for herpes simplex encephalitis is acyclovir, given intravenously at a dosage of 10 to 15 mg/kg every 8 hours, with each dose given over 1 hour.

Ganciclovir is an analogue of acyclovir which is active against all herpes viruses including Herpes simplex.

Vidarabine is a purine nucleoside analogue with activity against HSV-1, HSV-2, VZV, and EBV. Vidarabine inhibits viral DNA synthesis through its 5′-triphosphorylated metabolite

Amantadine is an antiviral agent whose dopaminergic properties make it effective in the treatment of Parkinson’s disease and for prophylaxis against the parkinsonian side effects of neuroleptic agents. It is not used in herpes simplex encephalitis.

Acyclovir is a synthetic deoxyguanosine analog and it is the prototype antiviral agent that is activated by viral thymidine kinase. The selective activity of aciclovir is due to its affinity for the thymidine kinase enzyme encoded by Herpes simplex (HSV) and Herpes Zoster (VZV).

Mechanism of action:HSV-1, HSV-2 and VZV thymidine kinase converts acyclovir to the acyclovir monophosphate, which is then converted to the diphosphate by cellular guanylate kinase, and finally to the triphosphate by phosphoglycerate kinase, phosphoenolpyruvate carboxykinase, and pyruvate kinase.

A young male presents with fever, followed by headache, confusion, focal seizures and right hemiparesis. MRI shows bilateral frontotemporal hyperintense lesion. Which of the following is the most likely diagnosis?

A

Acute pyogenic meningitis

B

Herpes simplex encephalitis

C

Neurocysticercosis

D

Carcinomatous meningitis

Q. 4

A young male presents with fever, followed by headache, confusion, focal seizures and right hemiparesis. MRI shows bilateral frontotemporal hyperintense lesion. Which of the following is the most likely diagnosis?

A

Acute pyogenic meningitis

B

Herpes simplex encephalitis

C

Neurocysticercosis

D

Carcinomatous meningitis

Ans.

B

Explanation:

Patient is showing features suggestive of herpes simplex encephalitis. Clinical manifestations in viral encephalitis includes altered level of consiousness (confusion, behavioral abnormalities), mild lethargy to coma, evidence of both focal or diffuse neurologic signs and symptoms and focal or generalized seizures.

Investigations: CSF shows lymphocytic leukocytosis, red blood cells due to hemorrhagic necrosis and elevated cerebrospinal fluid (CSF) protein levels. In HSV encephalitis80% will have abnormalities in temporal lobe and 10% have extra temporal abnormalities. The lesions are typically hyper intense on T2-weighted images. Brain biopsy has been the gold standard for defining HSV encephalitis, but now PCR for detection of HSV DNA in CSF has largely replaced biopsy for defining CNS infection. Acyclovir is used in the treatment.

These virus then migrates along nerve axons to sensory ganglia, and persists in a latent form and may be reactivated later.

In adults encephalitis is caused by HSV type 1.

In neonates HSV encephalitis is caused by type 2 virus during passage through the birth canal of a mother with active genital lesions.

HSV type 2 in adults causes meningitis, rather than encephalitis.

Ref: Clinical Neurology By Roger P. Simon, 7th Edition, Chapter 1

Q. 6

According to the latest evidence the latent virus infection which is responsible for the pathogenesis of the achalasia is:

A

Herpes simplex 1

B

Hepatitis C infection

C

Rubella

D

Measles

Q. 6

According to the latest evidence the latent virus infection which is responsible for the pathogenesis of the achalasia is:

A

Herpes simplex 1

B

Hepatitis C infection

C

Rubella

D

Measles

Ans.

A

Explanation:

It is believed that cause of ganglion cell degeneration in achalasia is an autoimmune process attributable to a latent infection with human herpes simplex virus 1 combined with genetic susceptibility.

Ref: Harrison, Edition-18, Page-2431.

Q. 7

In which one of the following infection dendritic ulcer is seen?

A

Herpes simplex

B

Measles

C

Pseudomonas

D

Gonococcal infection

Q. 7

In which one of the following infection dendritic ulcer is seen?

A

Herpes simplex

B

Measles

C

Pseudomonas

D

Gonococcal infection

Ans.

A

Explanation:

A dendritic corneal ulcer is the hallmark sign of HSV infection, accompanied by stromal keratitis in more severe infection. These ulcers may begin as nondescript punctate keratopathies but quickly coalesce to form the familiar branching patterns.

Because the virus invades and compromises the epithelial cells surrounding the ulcer, the leading edges (the so-called “terminal end-bulbs”) will stain with rose bengal or

lissamine green. Acyclovir 3% ointment is used as treatment.

Q. 8

Which of the following produces pocks on chorioallantoic membrane of chick embryo –

A

Myxovirus

B

Varicella

C

Herpes simplex

D

Cytomegalovirus

Q. 8

Which of the following produces pocks on chorioallantoic membrane of chick embryo –

Sensory supply of cornea is through trigeminal nerve Q. Neurotrophic keratopathy occurs due to paralysis of sensory supply of cornea. Causes of neurotrophic keratopathy or anaesthetic cornea are:

Q. 17

Which of the following statements about Mollaret meningitis is true?

A

Caused by Herpes simplex 2 in most of the cases.

B

Is a recurrent, benign septic meningitis

C

Is also referred to as “Benign Recurrent Neutrophilic Meningitis”

D

Does not resolve without treatment

Q. 17

Which of the following statements about Mollaret meningitis is true?

A

Caused by Herpes simplex 2 in most of the cases.

B

Is a recurrent, benign septic meningitis

C

Is also referred to as “Benign Recurrent Neutrophilic Meningitis”

D

Does not resolve without treatment

Ans.

A

Explanation:

Answer is A (Caused by Herpes simplex 2 in most of the cases):

Mollaret’s Meningitis is a form of Self-limiting Benign Recurrent Aseptic Lymphocvtic Meningitis that is most commonly caused by HSV-2 infection of the CNS.

Several etiologies have been proposed for Mollaret’s Meningitis however recent studies suggest that most cases of Mollaret’s Meningitis result from Herpes Simplex Virus -2 (HSV-2) infection

Mollaret’s Meningitis

It is the name given to a Self-Limited Recurrent form of Aseptic Meningitis

It is also referred to as Benign Recurrent Lymphocytic Meningitis

Recurrent episodes (typically> 3 episodes) of meningismus and fever lasting for 2-5 days with spontaneous resolution is highly suggestive of a diagnosis of Mollaret’s Meningitis

CSF Examination is characterized by a cloudy spinal fluid with lymphocytic pleocytosis and normal glucose and protein.

Presence of large granular cells on Papanicolaou’s stain of the CSF called `Mollaret’s Cells’ is considered pathognomonic (Mollaret’s cells were once thought to be endothelial cells but are now believed to be from the monocyte/ macrophage family)

Several etiologies. have been proposed for Mollaret’s Meningitis however recent studies suggest that most cases of Mollaret Meningitis result from Herpes Simplex Virus -2 (HSV-2) infection Presence of HSV DNA on PCR is highly suggestive of Mollaret’s Meningitis (In most cases HSV-2 DNA is detected

They are two members of the herpes virus family, Herpesviridae, that infect humans.

Both HSV-1 (which produces most cold sores) and HSV-2 (which produces most genital herpes) are ubiquitous and contagious.

They can be spread when an infected person is producing and shedding the virus.

Symptoms of herpes simplex virus infection include watery blisters in the skin or mucous membranes of the mouth, lips or genitals

Lesions heal with a scab characteristic of herpetic disease.

However, as neurotropic and neuroinvasive viruses, HSV-1 and -2 persist in the body by becoming latent and hiding from the immune system in the cell bodies of neurons.After the initial or primary infection, some infected people experience sporadic episodes of viral reactivation or outbreaks.

In an outbreak, the virus in a nerve cell becomes active and is transported via the neuron’s axon to the skin, where virus replication and shedding occur and cause new sores.